A range of molecular mechanisms have been investigated as possible explanations for corticosteroid insensitivity, including the overexpression of the dominant negative splice variant isoform GRβ which is associated with corticosteroid insensitivity in different cell types [41-43] and is reported to be increased in steroid resistant patients with asthma and ulcerative colitis [44-47]. The gene discussed is GZMB; the disease is asthma.